This section will provide information on Babesia (=Theileria) microti in Wisconsin. Wisconsin and Minnesota are hotspots for human babesiosis in the United States. The incidence in humans is increasing. Ixodes scapularis (deer ticks) are vectors for this disease.
Figure 1. Infection rates for Babesia microti in adult deer ticks collected through passive surveillance.
What is Babesisosis?
Human babesiosis is caused by microscopic protozoal parasites that infect red blood cells. Most human cases of babesiosis infection in the United States are caused by the parasite Babesia microti. Occasional cases in humans caused by other species (types) of Babesia have been detected (Herwaldt et al. 2012; Vannier and Krause 2012).
Taxonomic note: Most of the information available on this disease refers to Babesia microti as the causative agent. This species was renamed Theileria microti a few years ago. Recent genetic work suggests that it will be renamed again, with placement into a new genus. For these reasons, this website will maintain the Babesia name for the time being.
What is the status of human babesiosis in Wisconsin?
In Wisconsin, the number of reported cases has been increasing (see figure at right; courtesy of WDHS). The majority of the diagnosed cases occur in northwestern and west-central Wisconsin (see map on right; courtesy of WDHS). A review of all cases of human babesiosis reported to the Wisconsin Department of Health services during 1996-2005 was conducted by Pfeiffer et al. (2007). At least six patients were co-infected (infected at the same time) with other tick-borne pathogens (Pfieffer et al. 2007).
How is Babesia transmitted?
Babesia microti is most commonly transmitted or spread in nature by Ixodes scapularis ticks (also called blacklegged ticks or deer ticks). White-footed mice (Peromyscus leucopus) are considered the primary reservoir host of Babesia microti but other small rodents may play a role as reservoirs. Humans are accidental hosts (Vannier and Krause 2012; Steiner et al. 2008).
Babesia parasites can also be spread via:
- Blood transfusion from an infected donor–B. microti is the most common transfusion-transmitted infectious pathogen reported to the Food and Drug Administration (FDA) (Vannier and Krause 2012; Herwaldt et al. 2011; Leiby 2011).
- From an infected mother to her baby (congenital transmission) (Fox et al. 2006).
What are the Clinical Signs and Symptoms of Babesiosis?
Infection with Babesia sp. can range in severity from asymptomatic (no notable clinical signs or symptoms of illness) to severe or life-threatening. Symptoms, if any, usually develop within a few weeks or months after exposure but may first appear or recur many months later, particularly in persons who have a weak immune system (immunocompromised). The disease is usually more severe in people who are asplenic (do not have a spleen), immunocompromised or elderly (Vannier and Krause 2012).
Non-specific or flu-like symptoms include: fever, chills, headache, body aches, fatigue, loss of appetite and nausea.
Since babesia parasites infect and destroy red blood cells they may cause a reduction in the number of red blood cells which can lead to a certain type of anemia called”hemolytic anemia.” Other severe symptoms and complications of babesia may include: low platelets (thrombocytopenia), low and unstable blood pressure, dysfunction in the body’s ability to clot leading to blood clots and bleeding and malfunction of vital organs such as the kidneys, lungs and liver.
Due to non-specific clinical signs which often accompany infection with Babesia species, medical providers should consider babesiosis in areas where the infectious organisms which cause Lyme disease, anaplasmosis and babesiosis are all potentially carried by the same tick vector (Ixodes scapularis–the black legged tick). Medical providers should also consider babesiosis in patients whom Lyme disease or anaplasmosis has been diagnosed if more severe clinical signs develop or they have a poor response to standard antimicrobial therapy (Vannier and Krause 2012; Sweeney et al. 1998).
How is Babesiosis Diagnosed?
If you think you may have babesiosis or another tick-borne illness or may have been exposed to or bitten by a deer tick (Ixodes scapularis), which is known to transmit Babesia microti, please contact your physician or medical provider. Diagnosis of babesiosis in humans is based on a thorough medical history, possible exposure to established high-risk areas for babesiosis or the ticks which carry the pathogen and physician observed clinical signs and symptoms as well as accompanying diagnostic laboratory methods to support the diagnosis.
Infection with babesiosis is most commonly diagnosed by examining a sample of a patient’s blood or “blood smear” under a microscope for evidence of Babesia organisms in red blood cells (Teal et al. 2012; Vannier and Krause 2012).
The organism can also be directly detected both accurately and rapidly by molecular testing methods such as polymerase chain reaction (PCR) (Teal et al. 2012). PCR testing should only be performed in laboratories that are experienced with such testing methods. Babesia sp. may be detected indirectly by serologic testing but this method only provides supporting evidence of exposure to the organism or the body’s immune response via production of antibodies (Wormser et al. 2006).
How is Babesiosis Treated?
Infection with Babesia microti is both treatable and preventable. Most patients who are asymptomatic do not require treatment. For patients who are clinically ill, treatment is required for a minimum of 7-10 days with a combination of two medications that must be prescribed by a medical professional. Treatment regimens typically include:
- atovaquone and azithromycin OR
- clindamycin and quinine
Wisconsin Maps and figures courtesy of James Kazmierczak, DVM; Wisconsin Department of Health Services
Babesiosis and the U.S. Blood Supply
Centers for Disease Control and Prevention (CDC). http://www.cdc.gov/parasites/babesiosis/
Fox LM, Wingerter S, Ahmed A, et al. (2006). Neonatal babesiosis: case report and review of the literature. Pediatr Infect Dis J;25:169-173
Herwaldt BL, Montgomery S, Woodhall D, Bosserman EA. (2012). Babesiosis surveillance-18 states, 2011. MMWR; July 13, 2012 / 61(27);505-509
Herwaldt BL, Linden JV, Bosserman E, Young C, Olkowska D, Wilson M. Transfusion-associated babesiosis in the United States: a description of cases. Ann Intern Med 2011;155:509-19.
Krause PJ, Lepore T, Sikand VK, et al. (2000). Atovaquone and Azithromycin for the Treatment of Babesiosis. N Engl J Med 2000; 343:1454-1458. http://www.nejm.org/doi/full/10.1056/NEJM200011163432004
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Leiby DA. (2011). Transfusion-transmitted Babesia spp.: bulls-eye on Babesia microti. Clin Microbiol Rev; 24(1): 14-28. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021205/pdf/0022-10.pdf
Pfeiffer, CD, Kazmierczak, JJ. & Davis, JP. (2007). Epidemiologic Features of Human Babesiosis in Wisconsin, 1996-2005. Wisconsin Medical Journal, 106(4): 191-95. http://www.wisconsinmedicalsociety.org/_WMS/publications/wmj/issues/wmj_v106n4/Kazmierczak.pdf
Sweeney CJ, Ghassemi M, Agger WA, Persing DH. (1998). Coinfection with Babesia microti and Borrelia burgdorferi in a western Wisconsin resident. Mayo Clin Proc; 73(4): 338-41. http://download.journals.elsevierhealth.com/pdfs/journals/0025-6196/PIIS0025619611636999.pdf
Teal AE, Habura A, Ennis J, Keithly JS, Madison-Antenucci S. (2012). A new real-time PCR assay for improved detection of the parasite Babesia microti. J Clin Microbiol; 50(3): 903-8. Epub 2011 Dec 14. http://jcm.asm.org/content/50/3/903.full.pdf
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Wormser GP, Prasad A, Neuhaus E, Joshi S, Nowakowski J, Nelson J, Mittleman A, Aguero-Rosenfeld M, Topal J, Krause PJ. (2010). Emergence of resistance to azithromycin-atovaquone in immunocompromised patients with Babesia microti infection.Clinical Infectious Diseases;50:381–6
Wormser GP, Dattwyler RJ, Shapiro ED, et al. (2006). The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis;43:1089-134. Erratum in: Clin Infect Dis 2007;45:941. http://www.uphs.upenn.edu/bugdrug/antibiotic_manual/idsalyme06.pdf